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H. Toba - One of the best experts on this subject based on the ideXlab platform.

  • A 40-Gb/s/ch WDM transmission with SPM/XPM suppression through prechirping and dispersion management
    Journal of Lightwave Technology, 2000
    Co-Authors: A. Sano, Y Miyamoto, S. Kuwahara, H. Toba
    Abstract:

    This paper proposes to combine prechirping with dispersion management scheme in such a way as to suppress the power penalty induced by self-phase modulation (SPM) and cross-phase modulation (XPM) in 40-Gb/s per channel wavelength-division multiplexed (WDM) transmission systems with long-amplifier spacing. First, we show that the optimum total dispersion to minimize SPM depends on prechirping and the local dispersion of the transmission Fiber, unlike that for minimizing XPM. Next, it is shown that, by optimizing the combination of prechirping and local dispersion, these two optima can be made to match so as to improve the allowable maximum Fiber Input power. Finally, the operation of the proposed optimization scheme is confirmed experimentally, and 4/spl times/40-Gb/s WDM transmission over 400 km of nonzero dispersion-shifted Fiber (NZDSF) is demonstrated successfully with the Fiber Input power of +10 dBm/ch and 250 GHz channel spacing.

  • Fiber four wave mixing in multi amplifier systems with nonuniform chromatic dispersion
    Journal of Lightwave Technology, 1995
    Co-Authors: K Inoue, H. Toba
    Abstract:

    Fiber Fiber-wave mixing (FWM) is studied for multichannel multi-amplifier systems composed of short Fibers with different zero-dispersion wavelength. An analytical expression describing FWM in these systems is derived. Using the expression, crosstalk is calculated for various combinations of Fiber lengths, which are selected according to a random function, and allowable Fiber Input power is evaluated. The results show that the allowable Input power for nonuniform dispersion is larger than that for uniform dispersion by several dB, depending on system conditions. >

  • Crosstalk and power penalty due to Fiber four-wave mixing in multichannel transmissions
    Journal of Lightwave Technology, 1994
    Co-Authors: K Inoue, K. Nakanishi, H. Toba
    Abstract:

    The influence of Fiber four-wave mixing on multichannel transmissions is investigated. We present strict and approximate theoretical treatments for evaluating power penalty with intensity-modulated/direct-detection (IM/DD) and FSK/direct detection. A comparison of calculations shows that both methods yield the same result in the small penalty region. Using these treatments, power penalty and allowable Fiber Input power are derived for various system conditions. It is shown that the power penalty is not uniquely determined by the crosstalk level for CW lights, depending on the demodulation scheme and channel spacing, especially in the zero-dispersion wavelength region.

  • Influence of Fiber four-wave mixing on multichannel FSK direct detection transmission systems
    Journal of Lightwave Technology, 1992
    Co-Authors: K Inoue, H. Toba
    Abstract:

    The influence of Fiber four-wave mixing on multichannel FSK direct detection transmission is investigated. A theoretical study is presented for evaluating error rate performance when four-wave mixing lights are overlapped onto a signal channel. Experiments are carried out to examine the theoretical treatment. Based on these results, allowable Fiber Input power is estimated.

Ray W Turner - One of the best experts on this subject based on the ideXlab platform.

  • long term potentiation at the mossy Fiber granule cell relay invokes postsynaptic second messenger regulation of kv4 channels
    The Journal of Neuroscience, 2016
    Co-Authors: Arsalan P Rizwan, Gerald W Zamponi, Xiaoqin Zhan, Ray W Turner
    Abstract:

    Mossy Fiber afferents to cerebellar granule cells form the primary synaptic relay into cerebellum, providing an ideal site to process signal Inputs differentially. Mossy Fiber Input is known to exhibit a long-term potentiation (LTP) of synaptic efficacy through a combination of presynaptic and postsynaptic mechanisms. However, the specific postsynaptic mechanisms contributing to LTP of mossy Fiber Input is unknown. The current study tested the hypothesis that LTP induces a change in intrinsic membrane excitability of rat cerebellar granule cells through modification of Kv4 A-type potassium channels. We found that theta-burst stimulation of mossy Fiber Input in lobule 9 granule cells lowered the current threshold to spike and increases the gain of spike firing by 2- to 3-fold. The change in postsynaptic excitability was traced to hyperpolarizing shifts in both the half-inactivation and half-activation potentials of Kv4 that occurred upon coactivating NMDAR and group I metabotropic glutamatergic receptors. The effects of theta-burst stimulation on Kv4 channel control of the gain of spike firing depended on a signaling cascade leading to extracellular signal-related kinase activation. Under physiological conditions, LTP of synaptically evoked spike output was expressed preferentially for short bursts characteristic of sensory Input, helping to shape signal processing at the mossy Fiber–granule cell relay. SIGNIFICANCE STATEMENT Cerebellar granule cells receive mossy Fiber Inputs that convey information on different sensory modalities and feedback from descending cortical projections. Recent work suggests that signal processing across multiple cerebellar lobules is controlled differentially by postsynaptic ionic mechanisms at the level of granule cells. We found that long-term potentiation (LTP) of mossy Fiber Input invoked a large increase in granule cell excitability by modifying the biophysical properties of Kv4 channels through a specific signaling cascade. LTP of granule cell output became evident in response to bursts of mossy Fiber Input, revealing that Kv4 control of intrinsic excitability is modified to respond most effectively to patterns of afferent Input that are characteristic of physiological sensory patterns.

  • intermediate conductance calcium activated potassium channels modulate summation of parallel Fiber Input in cerebellar purkinje cells
    Proceedings of the National Academy of Sciences of the United States of America, 2012
    Co-Authors: Jordan D T Engbers, Dustin Anderson, Hadhimulya Asmara, Renata Rehak, Hamish W Mehaffey, Shahid Hameed, Bruce E Mckay, Mirna Kruskic, Gerald W Zamponi, Ray W Turner
    Abstract:

    Encoding sensory Input requires the expression of postsynaptic ion channels to transform key features of afferent Input to an appropriate pattern of spike output. Although Ca2+-activated K+ channels are known to control spike frequency in central neurons, Ca2+-activated K+ channels of intermediate conductance (KCa3.1) are believed to be restricted to peripheral neurons. We now report that cerebellar Purkinje cells express KCa3.1 channels, as evidenced through single-cell RT-PCR, immunocytochemistry, pharmacology, and single-channel recordings. Furthermore, KCa3.1 channels coimmunoprecipitate and interact with low voltage-activated Cav3.2 Ca2+ channels at the nanodomain level to support a previously undescribed transient voltage- and Ca2+-dependent current. As a result, subthreshold parallel Fiber excitatory postsynaptic potentials (EPSPs) activate Cav3 Ca2+ influx to trigger a KCa3.1-mediated regulation of the EPSP and subsequent after-hyperpolarization. The Cav3-KCa3.1 complex provides powerful control over temporal summation of EPSPs, effectively suppressing low frequencies of parallel Fiber Input. KCa3.1 channels thus contribute to a high-pass filter that allows Purkinje cells to respond preferentially to high-frequency parallel Fiber bursts characteristic of sensory Input.

  • IKCa-Cav3 complex creates a high pass filter for parallel Fiber Input in cerebellar Purkinje cells
    BMC Neuroscience, 2011
    Co-Authors: Jordan D T Engbers, Dustin Anderson, Renata Rehak, Hamish W Mehaffey, Bruce E Mckay, Mirna Kruskic, Gerald W Zamponi, Ray W Turner
    Abstract:

    Cerebellar Purkinje cells are contacted by up to ~150,000 parallel Fibers from granule cells, of which only a subset will convey sensory information at any given time. Purkinje cells must then possess the means to respond effectively to meaningful parallel Fiber Input over background noise. Previous work has shown that parallel Fiber excitatory postsynaptic potential (EPSP) summation can be shaped by feedforward synaptic inhibition and the hyperpolarization-activated current IH[1,2]. We now report that parallel Fiber EPSPs activate T-type calcium channels that are linked to intermediate conductance calcium-activated potassium (IKCa) channels in Purkinje cells. This novel complex exerts a frequency-dependent suppression of temporal summation, such that only high frequency parallel Fiber Inputs undergoing presynaptic facilitation can elicit spike output from Purkinje cells. Cerebellar slices were prepared from P18-30 rats and patch recordings obtained from PC somata at 32-35°C. PFs were activated using a monopolar stimulating electrode in the molecular layer or granule cell layer. Alternatively, the role of postsynaptic PC ion channels were selectively tested by injecting simulated EPSCs to evoke PF simulated EPSPs (simEPSPs) at the soma. PF EPSPs below threshold for spike discharge were followed by an after hyperpolarization (AHP) of up to 2.5 mV and 250 ms. Application of blockers against high voltage activated Ca2+ channels (Cd2+, Agatoxin IVA), SK channels (apamin), or BK channels (TEA, iberiotoxin, paxilline) did not significantly affect the rate of simEPSP decay. However, T-type Ca2+ channel blockers (Ni2+, Mibefradil, kurtoxin) caused a ~35% decrease in the rate of simEPSP decay. Moreover, these effects were reproduced by application of IKCa channel blockers (TRAM-34, charybdotoxin). Immunofluorescent labeling for IKCa protein confirmed its expression in Purkinje cells somata and dendrites. Ni2+ and TRAM-34 sensitive outward currents were found in outside-out patches from PC somata, confirming current clamp data showing a functional link between Cav3 and IKCa channels. The outward current was further blocked by BAPTA (10 mM) but not EGTA (10 mM) in the internal patch solution, indicating that the Ca2+-IKca channel interaction resides within a nanodomain. To examine the effect of this interaction on temporal summation, PFs were stimulated at varying frequencies. For frequencies up to 25 Hz, no temporal summation was observed in control conditions. However, blocking either Cav3 or IKca channels caused significant summation for 25 Hz stimulations. This effect was seen in both the presence and absence of feedforward-inhibition. Application of TRAM-34 greatly altered the frequency response of PC to 50 and 100 Hz PF stimulation during tonic firing. Finally, the Cav3-IKCa complex selectively suppresses non-facilitating Inputs while allowing smaller-amplitude, facilitating Inputs to generate output. Our current work is the first to demonstrate the expression of IKCa channels in central neurons, its association with Cav3 channels and the role of this Cav3-IKCa complex in controlling the response of PCs to PF Inputs. The Cav3-IKCa complex creates a high pass filter that reduces the effectiveness of background activity and allows Purkinje cells to respond preferentially to parallel Fiber Input indicative of sensory Input carried by mossy Fibers.

Michael Häusser - One of the best experts on this subject based on the ideXlab platform.

  • dendritic calcium signaling triggered by spontaneous and sensory evoked climbing Fiber Input to cerebellar purkinje cells in vivo
    The Journal of Neuroscience, 2011
    Co-Authors: Kazuo Kitamura, Michael Häusser
    Abstract:

    Cerebellar Purkinje cells have one of the most elaborate dendritic trees in the mammalian CNS, receiving excitatory synaptic Input from a single climbing Fiber (CF) and from ∼200,000 parallel Fibers. The dendritic Ca2+ signals triggered by activation of these Inputs are crucial for the induction of synaptic plasticity at both of these synaptic connections. We have investigated Ca2+ signaling in Purkinje cell dendrites in vivo by combining targeted somatic or dendritic patch-clamp recording with simultaneous two-photon microscopy. Both spontaneous and sensory-evoked CF Inputs triggered widespread Ca2+ signals throughout the dendritic tree that were detectable even in individual spines of the most distal spiny branchlets receiving parallel Fiber Input. The amplitude of these Ca2+ signals depended on dendritic location and could be modulated by membrane potential, reflecting modulation of dendritic spikes triggered by the CF Input. Furthermore, the variability of CF-triggered Ca2+ signals was regulated by GABAergic synaptic Input. These results indicate that dendritic Ca2+ signals triggered by sensory-evoked CF Input can act as associative signals for synaptic plasticity in Purkinje cells in vivo and may differentially modulate plasticity at parallel Fiber synapses depending on the location of synapses, firing state of the Purkinje cell, and ongoing GABAergic synaptic Input.

  • Dendritic spikes mediate negative synaptic gain control in cerebellar Purkinje cells
    Proceedings of the National Academy of Sciences of the United States of America, 2010
    Co-Authors: Ede A. Rancz, Michael Häusser
    Abstract:

    Dendritic spikes appear to be a ubiquitous feature of dendritic excitability. In cortical pyramidal neurons, dendritic spikes increase the efficacy of distal synapses, providing additional inward current to enhance axonal action potential (AP) output, thus increasing synaptic gain. In cerebellar Purkinje cells, dendritic spikes can trigger synaptic plasticity, but their influence on axonal output is not well understood. We have used simultaneous somatic and dendritic patch-clamp recordings to directly assess the impact of dendritic calcium spikes on axonal AP output of Purkinje cells. Dendritic spikes evoked by parallel Fiber Input triggered brief bursts of somatic APs, followed by pauses in spiking, which cancelled out the extra spikes in the burst. As a result, average output firing rates during trains of Input remained independent of the Input strength, thus flattening synaptic gain. We demonstrate that this “clamping” of AP output by the pause following dendritic spikes is due to activation of high conductance calcium-dependent potassium channels by dendritic spikes. Dendritic spikes in Purkinje cells, in contrast to pyramidal cells, thus have differential effects on temporally coded and rate coded information: increasing the impact of transient parallel Fiber Input, while depressing synaptic gain for sustained parallel Fiber Inputs.

  • The origin of the complex spike in cerebellar Purkinje cells.
    J Neurosci, 2008
    Co-Authors: Michael Häusser
    Abstract:

    Activation of the climbing Fiber Input powerfully excites cerebellar Purkinje cells via hundreds of widespread dendritic synapses, triggering dendritic spikes as well as a characteristic high-frequency burst of somatic spikes known as the complex spike. To investigate the relationship between dendritic spikes and the spikelets within the somatic complex spike, and to evaluate the importance of the dendritic distribution of climbing Fiber synapses, we made simultaneous somatic and dendritic patch-clamp recordings from Purkinje cells in cerebellar slices. Injection of large climbing Fiber-like synaptic conductances at the soma using dynamic clamp was sufficient to reproduce the complex spike, independently of dendritic spikes, indicating that neither a dendritic synaptic distribution nor dendritic spikes are required. Furthermore, we found that dendritic spikes are not directly linked to spikelets in the complex spike, and that each dendritic spike is associated with only 0.24 +/- 0.09 extra somatic spikelets. Rather, we demonstrate that dendritic spikes regulate the pause in firing that follows the complex spike. Finally, using dual somatic and axonal recording, we show that all spikelets in the complex spike are axonally generated. Thus, complex spike generation proceeds relatively independently of dendritic spikes, reflecting the dual functional role of climbing Fiber Input: triggering plasticity at dendritic synapses and generating a distinct output signal in the axon. The encoding of dendritic spiking by the post-complex spike pause provides a novel computational function for dendritic spikes, which could serve to link these two roles at the level of the target neurons in the deep cerebellar nuclei.

Tadashi Kawasaki - One of the best experts on this subject based on the ideXlab platform.

K Inoue - One of the best experts on this subject based on the ideXlab platform.